The mechanism of inhibitory effect of AMP kinase for aldosterone-induced vascular damage

我们成功地利用Tet-On表达系统建立了血管内皮特异性显性阴性（dn）和组成活性（ca） AMPK转基因小鼠。在dox处理的doca盐TEK-rtTA/TRE-caAMPK小鼠中，与对照doca盐小鼠相比，内皮依赖性血管舒张得到显著改善。L-NMMA预处理抑制eNOS完全抵消了这种改善作用。dox处理的doca盐TEK-rtTA/TRE-dnAMPK小鼠的内皮依赖性血管舒张明显减弱。三种doca盐小鼠（Wt, caAMPK, dnAMPK）的血压水平没有差异，表明AMPK的内皮保护作用是不依赖于bp的。

We succeeded in creating vascular-endothelium-specific dominant-negative (dn) and constitutively-active (ca) AMPK transgenic mice using Tet-On expression system. In DOX-treated DOCA-salt TEK-rtTA/TRE-caAMPK mice, endothelium-dependent vasodilatation was significantly ameliorated compared to control DOCA-salt mice. L-NMMA pretreatment to inhibit eNOS completely canceled such ameliorating effect. Endothelium-dependent vasodilatation was significantly attenuated in DOX-treated DOCA-salt TEK-rtTA/TRE-dnAMPK mice thanin control mice. The blood pressure levels of three types DOCA-salt mice (Wt, caAMPK, dnAMPK) were not different, suggesting that such endothelial-protective effect of AMPK was BP-independent.